Using the yeast Saccharomyces cerevisiae we are examining mitotically identified DNA repair systems during normal meiosis. Mutants in the UV and X-ray repair pathways are being used: rad1 (excision), rad52 (X-ray) and rad6 (mutational). The initiation of meiotic DNA synthesis is normal in the mutants and excision repair mutants are like wild type for the other aspects of meiosis: recombination, haploidization, and size of DNA. In rad6 and rad52 mutants, recombination is abolished and for rad52 the spore products are inviable. The rad52 mutant accumulates single-strand DNA breaks/gaps during meiotic DNA synthesis in both the parental and newly synthesized strands. The timing corresponds to the beginning of lethality: lethality and breaks are prevented by inhibitors of DNA synthesis. The frequency of breaks (about 200 per cell) approximates the number of genetic recombinational events. We conclude that the RAD52 gene product is involved with recombination and the breaks may be intermediates in this process. The breaks probably occur prior to homologous chromosomes pairing. It thus appears that the rad52 gene product is essential in normal meiosis and in protection from ionizing radiation damage; the mechanism of action involves recombination.